Rheumatoid Arthritis – Joint Pathology

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As joint is a very well engineered structure, frictionless motion is

provided by the combination of a smooth articular cartilage as well as

lubrication of both the articular cartilage and the synovial membrane

together which make up the entire surface area of the inside of the joints.

Shock absorption to the joint is provided by the combination of

structures, including articular cartilage, subchondral bone and soft tissue

structures (Joint Capsule and Ligaments). Because of its re-silent nature

and ability to compress, articular cartilage in itself is a good shock

absorber but its thickness and overall volume is far less than bone or soft

tissues. Hence the soft tissues and bones are the primary shock absorbers

in joint and any disease that affect bones or soft tissue is going to

interfere with this shock absorption. Re-silence of the soft tissue is

important for normal motion as well as shock absorption. Hyaluronic

acid provides lubrication to the synovial membrane surface in addition to

another protein structure called Lubricin and is involved in the lubrication

of articular cartilage. The substance moving over the surface of joints is

called Boundary Lubrication. A second mechanism of lubrication of

cartilage is effected by fluid being squeezed out of the cartilage on to the

surface when weight bearing occurs.

Rheumatoid arthritis embrace an amazing array of hereditary and

acquired disorder with a wide variety of clinical features.

The pathological hallmark of RA is synovial membrane

proliferation outgrowth associated with erosion of articular cartilage and

subchondral bone. In early stages, the most obvious histological changes

are confined to the synovial microvasculature which shows evidence of

endothelial damage, infilteration by polymorpho nuclear leucocytes and

obliteration by thrombus. In chronic phase, polymorpho nuclear

leucocytes are less obvious but the synovium is infilterated by large

number of inflammatory cells (macrophages, T&B lymphocytes,

dendritic cells, plasma cells). The plasma cells in the subsynovium

synthesize large quantities of immunoglobulin, much of which is IgM and

IgG rheumatoid factor. They have the ability to form immune complexes

that can activate complement and is important in either initiating or

prolonging local inflammation within the joint. Antigen-Antibody

complexes formed within the joint cavity can become trapped in hyaline

cartilage and fibrocartilage, where they cause changes in matrix macro

molecules. Ultimate destruction of cartilage, bone, tendons and ligaments

probably results from proteolytic enzymes, metallo proteinases.


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